AIM: To examine the effects of anti-high mobility group box 1 (HMGB1) neutralizing antibody in experimental se-vere acute pancreatitis (SAP).METHODS: SAP was induced by creating closed duode-nal loop in C3H/HeN mice. SAP was induced immediately after intraperitoneal injection of anti-HMGB1 neutralizing antibody (200 μg). Severity of pancreatitis, organ injury (liver, kidney and lung), and bacterial translocation to pancreas was examined 12 h after induction of SAP.RESULTS: Anti-HMGB1 neutralizing antibody significant-ly improved the elevation of the serum amylase level and the histological alterations of pancreas and lung in SAP. Anti-HMGB1 antibody also significantly ameliorated the elevations of serum alanine aminotransferase and cre-atinine in SAP. However, anti-HMGB1 antibody worsened the bacterial translocation to pancreas.CONCLUSION: Blockade of HMGB1 attenuated the development of SAP and associated organ dysfunction, suggesting that HMGB1 may act as a key mediator for inflammatory response and organ injury in SAP. AIM: To examine the effects of anti-high mobility group box 1 (HMGB1) neutralizing antibody in experimental se-vere acute pancreatitis (SAP). METHODS: SAP was induced by creating a closed closed duode-nal loop in C3H / HeN mice. induced immediately after intraperitoneal injection of anti-HMGB1 neutralizing antibody (200 μg). Severity of pancreatitis, organ injury (liver, kidney and lung), and bacterial translocation to pancreas was examined 12 h after induction of SAP. antibody significant-ly improved the elevation of the serum amylase level and the histological alterations of pancreas and lung in SAP. Anti-HMGB1 antibody also significantly ameliorated the elevations of serum alanine aminotransferase and cre-atinine in SAP. However, anti-HMGB1 antibody worsened the bacterial translocation to pancreas. CONCLUSION: Blockade of HMGB1 attenuated the development of SAP and associated organ dysfunction, suggesting that HMGB1 may act as a key mediator for inflammat ory response and organ injury in SAP.